Cardiology / English / General propedeutics of internal diseases_Nemtsov-LM_2016

or when he has nervous trembling, or diseases of the respiratory muscles, etc. Interrupted breathing over a limited part of the lung indicates difficult passage of air from small bronchi to the alveoli in this region and uneven unfolding of the alveoli. Interrupted breathing indicates pathology in fine bronchi and is more frequently heard at the apices of the lungs during their tuberculosis infiltration.

Bronchial breathing/respiration (laryngotracheal respiration)

Respiratory sounds known as bronchial or tubular breathing arise in the larynx and the trachea as air passes through the vocal slit. As air is inhaled, it passes through the vocal slit to enter wider trachea where it is set in vortextype motion. Sound waves thus generated propagate along the air column throughout the entire bronchial tree. Sounds generated by the vibration of these waves are harsh. During expiration, air also passes through the vocal slit to enter a wider space of the larynx where it is set in a vortex motion. But since the vocal slit is narrower during expiration, the respiratory sound becomes louder, harsher and longer. This type of breathing is called laryngotracheal (by the site of its generation).

Bronchial breathing is well heard in physiological cases over the larynx, the trachea, and at points of projection of the tracheal bifurcation (anteriorly, over the manubrium sterni, at the point of its junction with the sternum, and posteriorly in the interscapular space, at the level of the 3rd and 4th thoracic vertebrae). Bronchial breathing is not heard over the other parts of the chest because of large masses of the pulmonary tissue found between the bronchi and the chest wall.

Bronchial breathing can be heard instead of vesicular (or in addition to the vesicular breathing) over the chest in pulmonary pathology. This breathing is called pathological bronchial respiration.

It is conducted to the surface of the chest wall only under certain conditions, the main one being duration of the pulmonary tissue when the alveoli are filled with effusion (acute lobar pneumonia, tuberculosis, etc.), with blood (lung infarction), or due to compression of the alveoli by air or fluids accumulated in the pleural cavity, and compression of the lung against its root (compression atelectasis). In such cases the alveolar walls do not vibrate, while consolidated airless pulmonary tissue becomes a good conductor of sound waves in laryngotracheal respiration to the surface of the chest wall. Lungs may be consolidated due to replacement of the inflated pulmonary tissue by connective tissue (pneumosclerosis, carnification of the lung lobe, which sometimes occurs in acute lobar pneumonia, etc.).

Depending on degree of induration, its size and location in the lung, pathological bronchial breathing may have different intensity and pitch. If induration is large and superficial, loud bronchial breathing is heard as if near the ear. Bronchial breathing can be heard in acute lobar pneumonia at its

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second stadium (affection of the entire lobe of the lung). Especially soft and low sounds are heard inpatients with compression atelectasis.

Pathological bronchial breathing can be heard if an empty cavity is formed in the lung (abscess, cavern) and it is communicated with the bronchus. Consolidation of pulmonary tissue round the focus facilitates conduction of sound waves of laryngotracheal respiration to the surface of the chest wall, the more so that sound is intensified in the resonant cavity at the moment of air passage from narrow bronchus the air is set in vortex motion.

Depending the origin there are three types of pathological bronchial respiration:

1) Infiltrative type arises in consolidation of a pulmonary tissue (II stages of acute lobar pneumonia, infarct of lungs, tuberculosis),

2) Cavitary type is auscultated above superficially posed smooth-bore lumen of the big diameter connected with a bronchus (an abscess, a tubercular cavern, bronchiectasias with an appreciable distention of bronchi), 3) Atelectatic type - it is observed in compression atelectasis (exsudative pleurisy of 1,5-3 litres), is auscultated at a column on high bound of a dullness where is compressiated lung, rarely passes for lin. axillaries

anterior.

Amphoric respiration arises in the presence of a smooth-wall cavity (not less than 5-6 cm in diameter) communicated with a large bronchus. Sounds of this kind can be produced by blowing over the mouth of an empty glass or clay jar. This altered bronchial breathing is there called amphoric (Gk amphoeus jar).

Metallic respiration differs from both bronchial and amphoric. It is loud and high, and resembles the sound produced when a piece of metal is struck. Metallic respiration is heard in open pneumothorax when the air of the pleural cavity communicates with the external air.

Stenotic respiration is exaggerated laryngotracheal breathing which is heard in cases with narrowed trachea or large bronchus (due to a tumour); it is heard mainly ay points where physiological bronchial breathing is normally heard.

Bronchovesicular or mixed respiration is heard in lobular pneumonia or infiltrative tuberculosis, and also in pneumosclerosis, with foci of consolidated tissue being seated deeply in the pulmonary tissue and far from one another. Mixed breathing, when the inspiration phase is characteristic of vesicular breathing and the expiration phase of bronchial breathing, is often heard in such cases instead of weak bronchial breathing.

Adventitious sounds (additional respiratory sounds)

Adventitious sounds are rales, crepitation, and pleural friction.

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Rales arise in pathology of the trachea, bronchi, or if a cavern is formed in the affected lung. Rales are classified as dry (rhonchi) and moist rales.

Dry rales, or rhonchi, may be due to various causes. The main one is constriction of the lumen in the bronchi. Constriction may be total (in bronchial asthma), non-uniform (in bronchitis), or focal (in tuberculosis or tumour of the bronchus). Dry rales can be due to (1) spasms of smooth muscles of the bronchi during attacks of bronchial asthma; (2) swelling of the bronchial mucosa during its inflammation; (3) accumulation of viscous sputum in the bronchi which adheres to the wall of the bronchus and narrows its lumen; (4) formation of fibrous tissue in the walls of separate bronchi and in the pulmonary tissue with subsequent alteration of their architectonics (bronchiectasis, pneumosclerosis); (5) vibration of viscous sputum in the lumen of large and medium size bronchi during inspiration and expiration: being viscous, the sputum can be drawn (by the air stream) into threads which adhere to the opposite walls of the bronchi and vibrate like strings.

Dry rales are heard during inspiration and expiration and vary greatly in their loudness, tone and pitch. According to the quality and pitch of the sounds produced, dry rales are divided into sibilant rales (high-pitched and whistling sounds ,or ronchi sibilantes) and sonorous rales (low-pitched and sonoring sounds, or ronchi sonori). High-pitched rales are produced when the lumen of the small bronchi is narrowed, while low-pitched sonorous rales are generated in stenosis of medium caliber and large caliber bronchi or when viscous sputum is accumulated in their lumen.

Propagation and loudness of dry rales depend on the size of the affected area in the bronchial tree, on the depth of location of the affected bronchi, and the force of the respiratory movements. When the walls of a medium size and large bronchi are affected to a limited extent, rhonchi are insignificant and soft. Diffuse inflammation of the bronchi or bronchospasm arising during attacks of bronchial asthma is attended by both high-pitched sibilant and low-pitched sonorous rales which vary in tone and loudness. These rhonchi can be heard at a distance during expiration. If rhonchi are due to accumulation of viscous sputum in the bronchi, during deep breathing (or immediately after coughing) they can be either intensified or weakened, or else disappear altogether for a short time.

Moist rales are generated because of accumulation of liquid secretion (sputum, edematous fluid, blood) in the bronchi through which air passes. Air bubbles pass through the liquid secretion of the bronchial lumen and collapse to produce the specific cracking sound. This sound can be simulated by bubbling air through water using a fine tube. Moist rales are heard during both the inspiration and expiration, but since the air velocity is higher during inspiration, moist rales will be better heard at this respiratory phase.

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Depending on the caliber of bronchi where rales are generated, they are classified as fine, medium and coarse (large) bubbling rales. Fine bubbling rales are generated in fine bronchi and are percepted by the ear as short multiple sounds. Rales originating in the finest bronchi and bronchioles are similar to crepitation from which they should be differentiated (see below). Medium bubbling rales are produced in bronchi of a medium size and coarse bubbling rales in large caliber bronchi, in large bronchiectases, and in pulmonary cavities (abscess, cavern) containing liquid secretions and communicating with the large bronchus. Large bubbling rales are characterized by a lower and louder sound.

Moist rales originating in superficially located large cavities (5—6 cm and over in diameter) may acquire a metallic character. If segmentary bronchiectases or cavities are formed in the lung, rales can usually be heard over a limited area of the chest. Chronic bronchitis or marked congestion in the lungs associated with failure of the left chambers of the heart is as a rule attended by bilateral moist rales of various calibers, which occur at the symmetrical points of the lungs.

Depending on the character of the pathology in the lungs, moist rales are subdivided into consonating or crackling, and non-consonating or bubbling rales. Consonating moist rales are heard in the presence of liquid secretions in the bronchi surrounded by airless (consolidated) pulmonary tissue or in lung cavities with smooth walls surrounded by consolidated pulmonary tissue. The cavity itself acts as a resonator to intensify moist rales. Moist consonating rales are heard as if just outside the ear. Consonating rales in the lower portions of the lungs suggest inflammation of the pulmonary tissue surrounding the bronchi. Consonating rales heard in the subclavicular or subscapular regions indicate tuberculosis infiltration or cavern in the lung.

Non-consonating rales are heard in inflammation of bronchial mucosa (bronchitis) or acute edema of the lung due to the failure of the left chambers of the heart. The sounds produced by collapsing air bubbles in the bronchi are dampened by the "air cushion" of the lungs as they are conducted to the chest surface.

Crepitation

As distinct from rales, crepitation originates in the alveoli. Some authors erroneously classify these sounds as crepitant and subcrepitant rales. Crepitation is a slight crackling sound that can be imitated by rubbing a lock of hair. The main condition for generation of crepitation is accumulation of a small amount of liquid secretion in the alveoli. During expiration, the alveoli stick together, while during inspiration the alveolar walls are separated with difficulty and only at the end of the inspiratory movement. Crepitation is therefore only heard during the height of inspiration. In other words, crepitation is the sound produced by many alveoli during their simultaneous reinflation.

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Crepitation is mainly heard in inflammation of the pulmonary tissue, e.g. at the first (initial) and third (final) stages of acute lobar pneumonia, when the alveoli contain small amounts of inflammatory exudate, in infiltrative pulmonary tuberculosis, lung infarction, and finally in congestions that develop due to insufficient contractile function of the left-ventricular myocardium or in marked stenosis of the left venous orifice of the heart. Crepitation can be heard in the inferolateral portions of the lungs of aged persons during first deep inspirations, especially so if the patient was in the recumbent position before auscultation. The same temporary crepitation can be heard in compressive atelectasis. During pneumonia, crepitation is heard over longer periods and disappears when a large amount of inflammatory secretion is accumulated in the alveoli or after its complete resolution.

By its acoustic properties, crepitation can often resemble moist fine rales that are produced in fine bronchi or bronchioles filled with liquid secretion. Differentiation of moist rales from crepitation is of great diagnostic importance. Persistent crepitation may indicate pneumonia while fine nonconsonating rales suggest bronchitis.

Differential-diagnostic signs of these rales and crepitation are as follows: moist fine rales are heard during both inspiration and expiration; they can be intensified or disappear after coughing, while crepitation can only be heard at the height of inspiration; it does not change after coughing.

Pleural friction sounds (murmur)

In physiological conditions visceral and parietal layers of the pleura are constantly "lubricated" by pleural fluid and are therefore smooth. Their friction during breathing is noiseless. Various pathological conditions alter the physical properties of the pleural surfaces and their friction against one another becomes more intense to generate a peculiar adventitious noise, known as the pleural friction sound. Fibrin is deposited in inflamed pleura to make its surface rough; moreover, cicatrices, commissures, and bands are formed between pleural layers at the focus of inflammation. Tuberculosis and cancer are also responsible for the friction sounds.

Pleural friction sounds are heard during both inspiration and expiration. The sounds are differentiated by intensity, or loudness, length, and site over which they are heard. During early dry pleurisy the sounds are soft and can be imitated by rubbing silk or fingers in the close vicinity of the ear. The character of pleural friction sound is altered during the active course of dry pleurisy. It can resemble crepitation or fine bubbling rales (sometimes crackling of snow). In pleurisy with effusion, during the period of rapid resorption of exudate, the friction sound becomes coarser due to massive deposits on the pleural surfaces. This friction (to be more exact, vibrations of the chest) can be even identified by palpation of the chest.

The time during which pleural friction sound can be heard varies with diseases. For example, in rheumatic pleurisy pleural friction is only heard

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during a few hours; after a period of quiescence it reappears. Pleural friction persists for a week and over in dry pleurisy of tuberculosis etiology and pleurisy with effusion at the stage of resorption. Pleural friction sounds can be heard in some patients for years after pleurisy because of large cicatrices and roughness of the pleural surfaces.

The point over which pleural friction can be heard depends on the focus of inflammation. Most frequently it is heard in the inferolateral parts of the chest, where the lungs are most mobile during respiration. In rare cases this sound can be heard over the lung apices, when they are affected by tuberculosis with involvement of the pleural membranes.

If the inflammatory focus is localized in the pleura adjacent to the heart, pleuropericardial friction sound may be heard during both inspiration and expiration, and also during cardiac systole and diastole. As distinct from cardiac murmurs, this noise is best heard at the height of a deep inspiration because at that time the pleural surfaces come in closer contact with the pericardium.

Pleural friction sounds can be differentiated from fine bubbling rales and crepitation by the following signs: (1) the character of rales is altered or rales can disappear for a short time after coughing, while pleural friction sound does not change in these conditions; (2) when a stethoscope is pressed tighter against the chest, the pleural friction sound is intensified, while rales do not change; (3) crepitation is only heard at the height of inspiration, while pleural friction sound is heard during both inspiration and expiration; (4) if a patient moves his diaphragm in and out while his mouth and nose are closed, the sound produced by the friction of the pleura due to the movement of the diaphragm can be heard, while rales and crepitation cannot because there is no air movement in the bronchi.

Succusion (Hippocratic) sound. This is the splashing sound heard in the chest of a patient with hydropneumothorax, i.e. when serous fluid and air are accumulated in the pleural cavity. The sound was first described by Hippocrates, hence the name. The sound can be identified by auscultation: the physician presses his ear against the chest of the patient and then shakes the patient suddenly. The splashing sounds are sometimes heard by the patient himself during abrupt movements.

The so-called falling-drop sound (gutta cadens) can be heard by auscultation. It can occur in large cavities of the lungs or at the base of the pleural cavity which contain liquid pus or air as the patient changes his posture from recumbent to upright position or vice versa. Tenacious liquid containing pus sticks to the surface of the cavity and as the patient changes his position it gathers in drops which fall one after another into the liquid (sputum or pus) accumulated at the bottom.

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Bronchophony

This is the voice conduction by the larynx to the chest, as determined by auscultation. But as distinct from vocal fremitus, the words containing sounds “V” or “ch” are whispered during auscultation. In physiological conditions, voice conducted to the outer surface of the chest is hardly audible on either side of the chest in symmetrical points. Exaggerated bronchophony (like exaggerated vocal fremitus) suggests consolidation of the pulmonary tissue (which better conducts sound waves) and also cavities in the lungs which act as resonators to intensify the sounds. Bronchophony is more useful than vocal fremitus in revealing consolidation foci in the lungs of a patient with soft and high voice.

Examination of lung ventilation

The indices of lung ventilation are not constant and depend not only on the pathological conditions of the lungs or bronchi, but also on the patient's constitution, physical fitness, height, weight, sex, and age. The data obtained during examination of the patient are therefore assessed by comparing them with the data that might be expected from a person with the given physical properties. These data are calculated by special nomograms and formulas that have been compiled from basal metabolism indices.

Measuring respiratory capacity

Various indices are used to characterize lung ventilation. The so-called volumes of the lungs are most popular but they are not accurate enough.

1.The respiratory volume (RV) is the volume of air inspired and expired during normal breathing. It is 500 ml on the average varying from 300 to 900 ml. Of this volume, about 150 ml is the physiological dead-space volume of air (PDSV) which is present in the larynx, trachea, and bronchi, but which does not participate in art air to warm and moisten it, which makes residual air physiologically important.

2.The expiratory reserve volume (ERV) (1500-2000 ml). This is the

volume of air which can be expired by maximum effort after completion of a normal expiration.

3.The inspiratory reserve volume (IRV) (1500-2000 ml). This is the volume of air that can be inspired after a normal inspiration.

4.The vital capacity (VC) is found by summation of the IRV and ERV

and the respiratory volume (3700 ml on the average). This is the greatest volume of air that can be expired from the lungs after a maximum inspiration. The vital capacity of the lungs can be calculated by multiplying the tabulated (optimal) volume of basal metabolism by an empirically found factor 2.3. The deviation from the expected (optimum) vital capacity calculated by this method should not exceed ± 15 per cent.

5. The residual air volume (RAV) (1000-1500 ml) is the air that remains in the lungs after maximum expiration.

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6. The total lung capacity (TLC) is the sum of the RV, ERV and IRV, and RAV. It is about 5000-6000 ml.

Respiratory volumes can be used to assess possible compensation of respiratory insufficiency by increasing respiratory depth at the expense of expiration and inhalation and residual volume.

Normal respiratory volume is about 15 per cent of the vital lung capacity; expiratory and inspiratory air volumes are 42-43 per cent (inspiratory air usually slightly exceeds expiratory air volume); residual air is about 33 per cent of the vital capacity of the lungs. The VC slightly decreases in patients with obstructive hypoventilation, while expiratory and residual air volumes increase at the expense of decreased inspiratory air. RAV (especially the RAV: TLC ratio) increases in some cases to 50 per cent of the TLC (in lung emphysema, bronchial asthma, to a lesser degree in aged persons). VC in patients with hypoventilation also decreases because of the decreased IRV, while the RAV changes only insignificantly.

Spirography gives more reliable information on respiratory volumes. A spirograph can be used not only to measure various respiratory volumes but also some additional ventilation characteristics of intensity of lung ventilation such as the respiratory volume, minute volume, maximum ventilation of the lungs, and the volume of forced expiration.

Intensity of lung ventilation

1.The minute volume (MV) is calculated by multiplying the respiratory volume by respiratory rate; it is about 5000 ml on the average. More accurately the MV can be determined by a Douglas bag or using a spirograph.

2.The maximum lung ventilation (MLV) is the amount of air that can

be handled by the lungs by maximum effort of the respiratory system. It is determined by spirometry during deepest breathing at a rate of 50 r/min; normal ventilation is 80-200 1/min. According to Dembo, the predicted value of the maximum ventilation is the vital capacity of the lungs multiplied by 35 (MLV = VC x 35).

3. The respiratory reserve (RR) is determined by the formula RR = MLV - MV. In norm the RR exceeds the MV by at least 15-20 times. In healthy persons the RR is 85 per cent of the MLV, while in patients with respiratory insufficiency it decreases to 60 per cent or lower. This value shows the reserves of a healthy person by which he ensures adequate ventilation under considerable loads, or of a patient with respiratory insufficiency by which he may compensate for significant insufficiency by increasing the minute respiratory volume.

All these tests help study lung ventilation and its reserves, which are important when heavy work is done or there are respiratory diseases.

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Mechanics of the respiratory act

The study of this mechanics is necessary for determining changes in the inspiration to expiration ratio, the respiratory efforts at various respiratory phases, and other indices.

1.The forced expiratory vital capacity (FEVC). According to VotchalTiffeneau this is determined like the vital capacity except that the forced expiration should be performed as fast as possible. The FEVC is 8-11 per cent (100-300 ml) lower than the VC in healthy persons, mainly due to the increased resistance of fine bronchi to the passage of air. When this resistance increases due to bronchitis, bronchospasm, emphysema, etc., the difference may be as great as 1500 ml and more. The volume of forced expiration per minute is also determined. In healthy persons it is more than 75.0 per cent of the VC (average 82.7%).

2.The forced inspiratory vital capacity (FIVC) is determined during

forced inspiration at a maximum speed. It does not change in emphysema non-aggravated by bronchitis but decreases in obstructed patency of the airways.

3. Pneumotachymetry and peakflowmetry are the technique used for measuring peak velocities of air streams in forced inspiration and expiration and is intended to determine the condition of bronchial patency.

Types of disordered lung ventilation

Depending on the cause and mechanism of developing respiratory insufficiency, three types of disordered lung ventilation are distinguished: obstructive, restrictive and mixed (combined).

The obstructive type is characterized by difficult passage of air through the bronchi (because of bronchitis, bronchospasm, contraction or compression of the trachea or large bronchi, e.g. by a tumour, etc.). Spirography shows marked decrease in the MLV and FEVC, the VC being decreased insignificantly. Obstruction of the air passage increases the load on the respiratory muscles. The ability of the respiratory apparatus to perform additional functional load decreases (fast inspiration, and especially expiration, and also rapid breathing become impossible).

Airflow obstruction is usually determined by forced expiratory spirometry - the recording of exhaled volume against time during a maximal expiration. Normally, a full forced expiration takes between 3 and 4 sec, but when airflow is obstructed, it takes up to 15 or even 20 sec and may be limited by breath-holding time. The normal forced expiratory volume in the first second of expiration (FEV1) is easily measured and accurately predicted on the basis of age, sex, and height. The ratio of FEV1 to forced vital capacity (FEV1/FVC, or index of Tiffeneau) normally exceeds 0.75 (75%), in bronchial obstruction FEV1/FVC <0.7 (70%).

The restrictive type of ventilation disorder occurs in limited ability of the lungs to expand and to collapse, i.e. in pneumosclerosis, hydroand

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pneumothorax, massive pleural adhesions, kyphoscoliosis, ossification of the costal cartilages, limited mobility of the ribs, etc. These conditions are in the first instance attended by a limited depth of the maximum possible inspiration. In other words, the vital capacity of the lungs (VC) decreases together with the maximum lung ventilation (MLV), but the dynamics of the respiratory act is not affected: no obstacles to the rate of normal breathing (and whenever necessary, to significant acceleration of respiration) are imposed.

The mixed, or combined type includes the signs of the two previous disorders, often with prevalence of one of them; this type of disorder occurs in long-standing diseases of the lungs and the heart.

Examination of patients with diseases of circulatory system:

Subjective examination. Objective examination of circulatory system: survey and palpation of region of the heart and large vessels. Measuring arterial (blood) pressure

Inquiry

Complaints

Patients with diseases of the heart usually complain of dyspnea, i.e. distressing feeling of air deficit. Dyspnea is a sign of the developing circulatory insufficiency, the degree of dyspnea being a measure of this insufficiency. When questioning the patient, it is therefore necessary to find out the conditions under which dyspnea develops. At the initial stages of heart failure, dyspnea develops only during exercise, such as ascending the stairs or a hill, or during fast walk. Further, it arises at mildly increased physical activity, during talking, after meals, or during normal walk. In advanced heart failure, dyspnea is observed even at rest. Cardiac dyspnea is caused by some factors which stimulate the respiratory centre.

Attacks of asphyxia, which are known as cardiac asthma, should be differentiated from dyspnea. An attack of cardiac asthma usually arises suddenly, at rest, or soon after a physical or emotional stress, sometimes during night sleep. It may develop in the presence of dyspnea. In paroxysmal attacks of cardiac asthma, the patient would usually complain of acute lack of air; respiration becomes stertorous, the sputum is foamy with traces of blood.

Patients often complain of palpitation. They feel accelerated and intensified heart contractions. Palpitation is determined by the increased excitability of the patient's nerve apparatus that controls heart activity. Palpitation is a sign of affection of the heart muscle in cardiac diseases such as myocarditis, myocardial infarction, congenital heart diseases, etc., it may

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